الفهرس 
Title : Immuno protective effect of taurine against Amikacininduced nephrotoxicity in rats
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Abstract
One of the most potent aminoglycoside antibiotics is amikacin (AMK). However,
nephrotoxicity is a serious and dose-limiting adverse effect associated with its therapeutic
usage, particularly in patients receiving large doses of AMK. The purpose of this study was
to see if taurine (TAU) might relieve or prevent AMK-induced nephrotoxicity when
concurrent with AMK, with an emphasis on inflammation, apoptosis, and fibrosis. Six groups
of male Sprague Dawley rats were formed. group 1: rats received saline (normal control),
group 2: normal rats received 50 mg/kg TAU intraperitoneally (i.p.). Groups 3 and 4:
received AMK (25 or 50 mg/kg; i.p.), respectively. Groups 5 and 6: received TAU (50
mg/kg; i.p.) concurrently with AMK (25 or 50 mg/kg; i.p.) for 3 weeks, respectively. High
levels of serum creatinine (CRE), urea nitrogen (BUN) and uric acid (UA) were shown in
AMK-mediated nephrotoxicity. Renal tissue damage has determined during histopathological
studies. The development of inflammatory responses and localized fibrosis involves
increased degree of heat shock protein (HSP) 25 and Toll-like receptors-4 (TLR-4).
Improved TLR-4 enables monocytes to increase the production of interleukin (IL)-18 rather
than IL-10. TAU showed therapeutic effects against AMK-caused nephrotoxicity with the
downregulation of HSP25, TLR-4, caspase-3 and IL-18 with up-regulation IL-10 levels.